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Insulin-degrading enzyme

Insulysin, IDE, insulinase, insulin protease
This gene encodes a zinc metallopeptidase that degrades intracellular insulin, and thereby terminates insulins activity, as well as participating in intercellular peptide signalling by degrading diverse peptides such as glucagon, amylin, bradykinin, and kallidin. The preferential affinity of this enzyme for insulin results in insulin-mediated inhibition of the degradation of other peptides such as beta-amyloid. Deficiencies in this protein's function are associated with Alzheimer's disease and type 2 diabetes mellitus but mutations in this gene have not been shown to be causitive for these diseases. This protein localizes primarily to the cytoplasm but in some cell types localizes to the extracellular space, cell membrane, peroxisome, and mitochondrion. Alternative splicing results in multiple transcript variants encoding distinct isoforms. Additional transcript variants have been described but have not been experimentally verified.[provided by RefSeq, Sep 2009] (from NCBI)
Top mentioned proteins: Insulin, CAN, APP, ACID, HAD
Papers on Insulysin
Efficient attenuation of Friedreich's ataxia (FRDA) cardiomyopathy by modulation of iron homeostasis-human induced pluripotent stem cell (hiPSC) as a drug screening platform for FRDA.
Ho et al., Hong Kong, Hong Kong. In Int J Cardiol, Feb 2016
METHODS: Application of our previously established FRDA human induced pluripotent stem cell (hiPSC) derived cardiomyocytes model as a platform to assess the efficacy of treatment with either the antioxidant coenzyme Q10 analog, idebenone (IDE) or the iron chelator, deferiprone (DFP), which are both under clinical trial.
Targeting Insulin-Degrading Enzyme to Treat Type 2 Diabetes Mellitus.
Tang, Chicago, United States. In Trends Endocrinol Metab, Jan 2016
Insulin-degrading enzyme (IDE) selectively degrades peptides, such as insulin, amylin, and amyloid β (Aβ) that form toxic aggregates, to maintain proteostasis.
Changes in astrocyte functional markers and β-amyloid metabolism-related proteins in the early stages of hypercholesterolemia.
Xiao et al., Nanjing, China. In Neuroscience, Jan 2016
Levels of Aβ, and its precursor protein, were unaffected, but levels of presenilin 1 and insulin-degrading enzyme (IDE), that initiate Aβ generation and degradation, respectively, increased in the hippocampus of the model mice.
Inhibitory Effect of Memantine on Streptozotocin-Induced Insulin Receptor Dysfunction, Neuroinflammation, Amyloidogenesis, and Neurotrophic Factor Decline in Astrocytes.
Shukla et al., Lucknow, India. In Mol Neurobiol, Jan 2016
STZ (100 μM) treatment for 24 h in astrocytes resulted significant decrease in brain-derived neurotrophic factor (BDNF), glial cell line-derived neurotrophic factor (GDNF), and insulin-degrading enzyme (IDE) expression in astrocytes.
Elevated glucose and oligomeric β-amyloid disrupt synapses via a common pathway of aberrant protein S-nitrosylation.
Lipton et al., Los Angeles, United States. In Nat Commun, Dec 2015
The increase in NO results in S-nitrosylation of insulin-degrading enzyme (IDE) and dynamin-related protein 1 (Drp1), thus inhibiting insulin and Aβ catabolism as well as hyperactivating mitochondrial fission machinery.
Impact of Insulin Degrading Enzyme and Neprilysin in Alzheimer's Disease Biology: Characterization of Putative Cognates for Therapeutic Applications.
Kumar et al., Delhi, India. In J Alzheimers Dis, Nov 2015
This purpose is expertly fulfilled by the potential role of Aβ degrading enzymes such as insulin degrading enzyme (IDE) and Neprilysin (NEP).
Enhanced Phospholipase A2 Group 3 Expression by Oxidative Stress Decreases the Insulin-Degrading Enzyme.
Yokota et al., Tokyo, Japan. In Plos One, 2014
We previously reported that Alzheimer disease (AD) model mice showed decreased insulin-degrading enzyme (IDE) levels in the cerebrum and accelerated phenotypic features of AD when crossbred with alpha-tocopherol transfer protein knockout (Ttpa-/-) mice.
Environmental pollutants as risk factors for neurodegenerative disorders: Alzheimer and Parkinson diseases.
Quintanilla-Vega et al., Mexico. In Front Cell Neurosci, 2014
Common mechanisms of environmental pollutants to increase Aβ, P-Tau, α-syn and neuronal death have been reported, including the oxidative stress mainly involved in the increase of Aβ and α-syn, and the reduced activity/protein levels of Aβ degrading enzyme (IDE)s such as neprilysin or insulin IDE.
Insulin-degrading enzyme inhibition, a novel therapy for type 2 diabetes?
Butler et al., Los Angeles, United States. In Cell Metab, 2014
The insulin-degrading enzyme (IDE) has been identified as a type 2 diabetes and Alzheimer's disease susceptibility gene, though its physiological function remains unclear.
Anti-diabetic activity of insulin-degrading enzyme inhibitors mediated by multiple hormones.
Liu et al., Cambridge, United States. In Nature, 2014
Despite decades of speculation that inhibiting endogenous insulin degradation might treat type-2 diabetes, and the identification of IDE (insulin-degrading enzyme) as a diabetes susceptibility gene, the relationship between the activity of the zinc metalloprotein IDE and glucose homeostasis remains unclear.
Amyloid-clearing proteins and their epigenetic regulation as a therapeutic target in Alzheimer's disease.
Turner et al., Leeds, United Kingdom. In Front Aging Neurosci, 2013
A distinct metallopeptidase, insulin-degrading enzyme (IDE), also contributes to Aβ degradation in the brain.
ML345, A Small-Molecule Inhibitor of the Insulin-Degrading Enzyme (IDE)
Hodder et al., Bethesda, United States. In Unknown Journal, 2013
Insulin-degrading enzyme (IDE) is a thiol-sensitive zinc-metallopeptidase that is strongly implicated in the pathogenesis of multiple highly prevalent diseases, including type 2 diabetes and Alzheimer’s disease (AD).
Peptidomics approach to elucidate the proteolytic regulation of bioactive peptides.
Saghatelian et al., Seoul, South Korea. In Proc Natl Acad Sci U S A, 2012
Data show that in the absence of insulin-degrading enzyme (IDE), full-length calcitonin gene-related peptide (CGRP) levels are elevated in vivo.
Phosphorylation of amyloid-β peptide at serine 8 attenuates its clearance via insulin-degrading and angiotensin-converting enzymes.
Walter et al., Bonn, Germany. In J Biol Chem, 2012
Phosphorylation of amyloid-beta peptide at serine 8 attenuates its clearance via insulin-degrading and angiotensin-converting enzymes.
Nitric oxide decreases the enzymatic activity of insulin degrading enzyme in APP/PS1 mice.
Heneka et al., Bonn, Germany. In J Neuroimmune Pharmacol, 2012
These data suggest that NOS2 upregulation impairs amyloid beta degradation through negative regulation of insulin degrading enzyme
Somatostatin modulates insulin-degrading-enzyme metabolism: implications for the regulation of microglia activity in AD.
Marini et al., Roma, Italy. In Plos One, 2011
role played by somatostatin in preventing Abeta accumulation by partially restoring IDE activity
Disorder-specific effects of polymorphisms at opposing ends of the Insulin Degrading Enzyme gene.
Grünblatt et al., Würzburg, Germany. In Bmc Med Genet, 2010
The upstream polymorphism IDE2 was found to influence AD risk and to trigger the Abeta42 plasma level, whereas the downstream polymorphism IDE7 modified the T2DM risk; no associations were found for the intronic variant IDE9.
Production of an antigenic peptide by insulin-degrading enzyme.
Van den Eynde et al., Brussels, Belgium. In Nat Immunol, 2010
produce tumor antigenic peptides presented by MHC class I molecules for cytotoxic T lymphocyte recognition
Can the genetics of type 1 and type 2 diabetes shed light on the genetics of latent autoimmune diabetes in adults?
Schwartz et al., Philadelphia, United States. In Endocr Rev, 2010
For instance, no conclusive support for a role of the T1D-associated INS gene has been reported in T2D; conversely, but similarly, no evidence has been found for the role of the T2D-associated genes IDE/HHEX, SLC30A8, CDKAL1, CDKN2A/B, IGF2BP2, FTO, and TCF7L2 in T1D.
A genome-wide association study identifies novel risk loci for type 2 diabetes.
Froguel et al., Montréal, Canada. In Nature, 2007
These loci include a non-synonymous polymorphism in the zinc transporter SLC30A8, which is expressed exclusively in insulin-producing beta-cells, and two linkage disequilibrium blocks that contain genes potentially involved in beta-cell development or function (IDE-KIF11-HHEX and EXT2-ALX4).
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